VERIFIABLE CPD PAPER GENERAL

Rheumatoid arthritis – an update for

general dental practitioners
S. de Souza,*1 R. K. Bansal2 and J. Galloway3

InInbrief
brief
Updates dentists about rheumatoid arthritis and its Highlights oral conditions associated with rheumatoid Provides guidance for the management of rheumatoid
medical management. arthritis. arthritis patients in general dental practice.

Rheumatoid arthritis (RA) is a common chronic inflammatory autoimmune disorder which significantly impacts patients’ lives
and can lead to permanent disability. Inflammation in RA not only affects joints; but can affect organs including the heart
and lungs. Early diagnosis, initiation of intensive drug therapy, and a multidisciplinary care approach have vastly improved the
long-term prognosis for those living with the condition. However, RA patients often present with co-morbidities which add to
the complexity of clinical management. Orofacial conditions associated with RA which dental professionals need to be aware
of include periodontal disease, temporomandibular dysfunction and salivary gland dysfunction. In this article, we provide
information on RA, oral health in RA and guidance on how best to manage patients with RA in general dental practice.

Background
Rheumatoid arthritis (RA) is a common
chronic inflammatory autoimmune condition
which affects an estimated 400,000 UK adults.1
Onset is commonly between 40–50 years old,
though can occur at any age, with women three
times more likely affected than men.1 RA is a
common cause of disability; work disability
increases with age and disease duration.2 RA
results in increased healthcare costs and use
of social security provision, as well as signifi-
cantly reducing a patient’s quality of life.3,4
Pathophysiology
RA is characterised by the production of
rheumatoid factor (RF) and anti-citrullinated
1
Honorary Patient Expert, Academic Rheumatology, King’s
College London, London; 2General Dental Practitioner,
Springfield Dental Practice, Chelmsford and MSc Student,
Dental Institute, King’s College London, London; 3Senior
Clinical Lecturer, Academic Rheumatology, King’s College
London, London and Honorary Consultant Rheumatologist,
Rheumatology, King’s College Hospital NHS Foundation
Trust, London
*Correspondence to: Dr Savia de Souza
Address: Department of Academic Rheumatology and Clini-
cal Trials Group, Third Floor, Weston Education Centre, 10
Cutcombe Road, London, SE5 9RJ
Email: savia.de_souza@kcl.ac.uk
Refereed Paper. Accepted 15 August 2016
DOI: 10.1038/sj.bdj.2016.866
©
British Dental Journal 2016; 221: 667-673
protein antibodies (ACPAs) against autoanti-
gens commonly expressed within and outside
of synovial joints.5 RF is produced by B cells
in the synovial membrane and is associated
with more aggressive joint destruction. 6
Traditionally, RF was the classic autoanti-
body in RA; however, ACPAs are now seen
as being of increased importance as they are
more specific and sensitive for RA diagnosis
and predict a poorer disease course with pro-
gressive joint damage.7 RF, ACPA or both are
present in 50–80% of people with RA.7
RA has several distinct disease subsets with
several inflammatory cascades all resulting in
persistent synovial inflammation with damage
to articular cartilage and underlying bone.7 Key
inflammatory cytokines in its pathogenesis
are tumour necrosis factor alpha (TNF-α) and
interleukins 1 and 6 (IL-1, IL-6), which result
in the production of proteolytic enzymes and
activation of osteoclasts.6–8
Aetiology
It is thought RA occurs in response to environ-
mental triggers in genetically susceptible individ-
uals.5 The most recognised environmental trigger
is smoking, which increases levels of the peptidyl
arginine deiminase (PAD) enzyme responsible
for protein citrullination (the conversion of
arginine to citrulline).9 A recent study identi-
fied a clear dose-response relationship between
smoking and the risk of developing RA.10 The
periodontal pathogen Porphyromonas gingivalis
has been implicated in the aetiology of RA as
has, most recently, the gut microbiome.11,12 Other
suggested environmental risk factors include
region of birth, birthweight, breastfeeding and
socioeconomic status.13 Genetic factors account
for 50% of the risk of RA development, with more
than 100 loci for genetic susceptibility identified
to date.14,15 ACPA presence is associated with
alleles containing a shared epitope (common
protein-binding motif) in the HLA-DRB1 locus,
and can be detected up to 15 years before RA
onset.16,17
Signs and symptoms
Common clinical features of RA include a
symmetric polyarthritis with joint swelling
(particularly in the hands and feet).18 Persistent
joint inflammation (synovitis) results in bone
and cartilage destruction which can ultimately
lead to deformity, chronic pain and a loss of
function.9 Patients can experience stiffness
upon waking or after prolonged periods of
rest.18,19 Systemic inflammation in RA can
affect the brain (fatigue, reduced cognitive
function and cerebrovascular events), liver
(elevated acute-phase response and anaemia),
heart (myocardial infarction and cardiac
failure), lungs (inflammatory and fibrotic
diseases), exocrine glands (secondary Sjögren’s

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syndrome), bone (osteoporosis) and muscles
(sarcopenia).20 In severe RA, subcutaneous
nodules and other extra-articular manifesta-
tions (such as vasculitis) can develop.18
Diagnosis
In 2010, the European League Against
Rheumatism (EULAR) and the American
College of Rheumatology (ACR) jointly
released new classification criteria for RA
to assist rheumatologists with the diagnosis
of newly-presenting patients.21 This assesses
joint involvement, autoantibody status, acute-
phase reactants and symptom duration.7
Early diagnosis and initiation of intensive
treatment prevents joint damage, and greatly
improves functional outcome and morbidity
for patients.18
Clinical assessment
Disease activity is often assessed using combined
indices such as the Disease Activity Score, based
on the 28 joint count (DAS-28) which assesses
joints in the hands, arms and knees for swelling
and tenderness; measures the erythrocyte
sedimentation rate (an inflammatory marker),
and the patient’s global assessment (a visual
analogue scale-based score the patient gives for
how RA is affecting them overall at that time).6
The Simplified Disease Dctivity index (SDAI) or
the Clinical Disease Activity index (CDAI) are
alternatives.6 X-rays, ultrasound and magnetic
resonance imaging are all used to assess struc-
tural changes in the joints.6
Medical management
inflammatory pathway.6 Biologic DMARDs are
given to patients with persistently active disease,
and are highly effective.22 They are usually
prescribed for use in combination with metho-
trexate, as it is thought that this both reduces
antibody formation to the biologic agent and
increases its efficacy.7 Smoking reduces the
efficacy of conventional DMARDs and smokers
are more likely to fail on biologic therapies.24
In RA, the pain response appears to be
heightened; analgesics and non-steroidal
anti-inflammatory drugs (NSAIDs) can be
used for additional symptom control.7,25 Due
to unfavourable side-effects, corticosteroid
use is restricted to bridging therapy during
acute flares of symptoms (‘flare-ups’) whilst
awaiting DMARDs to reach full efficacy.7
Intra-articular injections are highly effective
for disease suppression in individual active
joints.7 New biologic DMARDs are currently
Table 1 Drugs commonly used in RA management6,22
Drug class Generic names
Paracetamol
Co-codamol
Analgesics
Co-dydramol
Tramadol
Ibuprofen
NSAIDs Naproxen
Diclofenac
Prednisolone
Corticosteroids
Methylprednisolone
in development, whilst biosimilar drugs
and novel small molecule agents have come
onto the market.6,22,26 The long-term effect of
these drugs in clinical practice is yet to be
determined. See Table 1 for a list of the most
common drugs currently used to manage RA.
Having RA increases the risk of infections
and this is raised further with the use of
biologics.6 Biologic DMARDs have approxi-
mately a 30% increased chance of serious
infection (for example, tuberculosis) over
conventional DMARD use, with this risk
at its highest during the first six months of
therapy.27,28 Other infection risks are bacterial
(for example, sepsis, abscesses and cellulitis),
fungal (for example, candidosis) and viral
(for example, shingles).7,29 Although there has
been speculation about an increased risk of
developing cancer with biologics use, a recent
systematic review has shown this to be little or

The aim of drug therapy is to reduce symptoms Methotrexate

and suppress inflammation, thereby limiting
Leflunomide
joint damage and disability.22 Currently, it Conventional DMARDs
is recommended to follow a ‘treat-to-target’ Sulfasalazine
strategy which involves initiating intensive drug Hydroxychloroquine
therapy immediately after diagnosis and escalat-
Adalimumab
ing this, guided by disease activity assessment,
until clinical remission or low disease activity is Etanercept
achieved.20,22 Disease-modifying anti-rheumatic Infliximab TNF inhibitors
drugs (DMARDs) are the primary treatment
Certolizumab pegol
used as they reduce pain and swelling of the Biologic DMARDs
joints, lower levels of acute-phase inflammatory Golimumab
markers, limit progressive joint damage and Rituximab – B-cell depletor
improve function.7 The first DMARD usually
Abatacept – T-cell costimulation inhibitor
prescribed is methotrexate (sulfasalazine or
leflunomide can be given if methotrexate is Tocilizumab – IL-6 inhibitor
contraindicated).7 DMARDs can be used in Tofacitinib – JAK inhibitor
combination to be more effective.23 Small molecule agents
Conventional DMARDs modify the whole [More to be licensed]

immune system, whereas biologic DMARDs NSAIDs = Non-steroidal anti-inflammatory drugs; DMARDs = Disease-modifying anti-rheumatic drugs; TNF = Tumour necrosis
factor; IL-6 = Interleukin-6; JAK = Janus kinase.
target specific components within the

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none.30 In future, it may be possible to taper
biologic DMARDs in select patients whose RA
is in remission.31
Improved management of RA over the
past two decades has resulted in a decline in
its severity with less inflammatory biomark-
ers, extra-articular manifestations, hospital
admissions and joint replacements.7 As better
therapies have resulted in the reduction or
absence of deformities, RA patients can appear
quite ‘normal’.32 For effective RA management,
adjunct non-pharmacologic interventions are
also advised (such as patient education, physi-
otherapy, occupational therapy, foot care and
psychological support) which are delivered
by a multidisciplinary team of healthcare
professionals.33
Co-morbidities
Co-morbid conditions can be coincidental
(with some already present at RA diagnosis),
reflective of RA or its treatment.34 RA patients
have excess mortality from cardiovascular
disease (CVD), but it remains unclear whether
cardiovascular events are caused by inflamma-
tion associated with RA rather than traditional
cardiac risk factors (such as hypertension,
dyslipidemia and cigarette smoking). 35,36
DMARDs are associated with a decreased risk
of all cardiovascular events but this is increased
with use of NSAIDs and corticosteroids.37
After CVD, the second most common cause
of mortality in RA is from cancer, particularly
lymphoma and lung cancer.38,39 Patients with
RA are more likely to develop skin cancer
(non-melanoma and possibly melanoma)
than the general population, and this risk
may be increased by DMARD use.40–42 RA
patients have an increased risk of osteoporo-
sis and resultant bone fractures linked to age,
disease duration and steroid therapy.38 Other
co-morbidities include anaemia, depression,
fibromyalgia, interstitial lung disease, Sjögren’s
syndrome, periodontal disease, diabetes
mellitus and obesity.7,34,38,39,43–46
It was previously reported that RA patients
die prematurely from one or more comorbid
diseases.47 However, a recent study found that
people who had RA onset after 2000, no longer
have an increased risk of mortality compared
to the general population.48 This is likely due
to improved treatments and tighter disease
control over the last two decades. Overall,
comorbidities increase disability levels, reduce
a patient’s quality of life, make patient manage-
ment more complex and increase the economic
burden of disease.34,38
Oral health
Oral health complications due to RA and its
treatments can cause additional problems for
patients. A recent study found that approxi-
mately 30% of RA patients were taking addi-
tional analgesics specifically for oral pain.49
Due to their immunosuppressive effects, RA
medications can promote periodontitis, can-
didosis and oral ulceration aided by a lack of
saliva.50 The three main oral conditions associ-
ated with RA are discussed below.
Periodontal disease
Periodontal disease (PD) is a chronic inflam-
matory condition which leads to destruction
of the periodontal ligament and alveolar
bone, and can result in tooth loss.51 PD is
caused by the presence of pathogenic gram-
negative anaerobic bacteria within the biofilm
attached to the sub-gingival tooth surface.9
Porphyromonas gingivalis (Pg) is the main
pathogen in PD.9 Its virulence combined with
an intense host immune response is thought to
contribute to the severity of the disease.9
People with RA are almost twice as likely
to have PD than those without.52 RA patients
with severe PD have significantly higher
DAS-28 scores than those with moderate or
no periodontitis, and PD is associated with
increased radiographic joint damage.53,54 These
data strongly suggest an association between
RA and PD/tooth loss. This association is
independent of common risk factors such as
smoking, alcohol intake, socioeconomic back-
ground and poor oral hygiene.55
RA and PD are both chronic inflammatory
diseases. Both conditions feature excessive
destruction of collagen-rich tissues: in RA
these are bone, cartilage and other periar-
ticular tissues; in PD these are alveolar bone,
periodontal ligament and gingiva.56 Alveolar
bone loss in PD results from the activation of
osteoclasts and is very similar to bone erosion
in RA, which is caused by cytokine-driven
osteoclast activation.9
PD may be involved in the initiation and/
or maintenance of systemic inflammation in
RA.9 The level of Pg antibodies has been found
to positively correlate with levels of ACPA in
circulation in RA.57 Pg is the only bacterium
known to express a PAD enzyme, which can
cause the citrullination of bacterial and host
proteins.58 This is thought to cause the body to
produce ACPA, which drives the autoimmune
response in RA.58 PAD enzymes, citrullinated
proteins and ACPA have all been found in
inflamed gingiva.59,60 Antibodies to the peri-
odontal pathogens Pg and Prevotella interme-
dia have been found in the serum and synovial
fluid of patients whose RA is active.61,62
Effective control of PD for RA patients is
important to reduce both local and systemic
inflammation, and the likelihood of bacterae-
mia.63 Persistent periodontitis can also reduce
the effectiveness of TNF inhibitors.64 Short-
term clinical trials have demonstrated that non-
surgical periodontal therapy in RA patients
with PD, can decrease RA disease activity
and systemic inflammation.65–67 Reduction
in disease activity may be due to less inflam-
matory products, bacteria and endotoxins in
the bloodstream after periodontal treatment,
thereby reducing the exposure of joints to
these products.68,69 Longer-term clinical trials
are currently in progress to find out whether
non-surgical periodontal treatment can lead
to an improvement in clinical outcomes and
quality of life for patients with active RA.70
A recent systematic review also highlighted
the importance of smoking cessation, which
results in improved outcomes for non-surgical
periodontal therapy.71
Temporomandibular dysfunction
The temporomandibular joint (TMJ) is used up
to 2,000 times a day for chewing and speaking,
making it one of the most frequently used
synovial joints in the body.72 People with RA
have a higher frequency and greater severity of
temporomandibular dysfunction (TMD) than
the normal population.73 The estimated preva-
lence of TMJ symptoms in adults with RA is
between 5–86% (depending on diagnostic
criteria, assessment methods and the popula-
tion studied) with clinical involvement of the
TMJ seen in about 50% of cases.73,74 In a 2013
survey of RA outpatients at a tertiary centre,
45.8% had problems with chewing (with 40.3%
having to adjust their diet accordingly), 30.6%
felt discomfort when eating and 36.1% took
medication to relieve oral pain.49
RA patients with TMD may present with
pain, difficulty with opening the mouth,
‘locking’ of the jaw, tenderness of the TMJ/
masticatory muscles, and joint sounds.73,75 The
most frequent joint sound is clicking, followed
by crepitus (which indicates TMJ degeneration
but may be seen less often due to improved
RA medication).76 It is thought that pain in
TMD is associated with RA disease activity,
and impairment in the range of motion and
function of the TMJ are more likely due to
degeneration of the joint.73 Patients may also

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report associated symptoms such as ear pain/

stuffiness, tinnitus, dizziness, headache and
neck pain.77 It is important to note that the TMJ
may already be affected by RA in patients who
do not yet report TMD symptoms.78
Clinical signs of TMJ involvement include
swelling, reduced range of motion and/or
deviation of the mandible to the affected side.75
Imaging shows condylar resorption with a
resultant shortening of the mandibular ramus-
condyle unit and possibly a reduced joint
space.77 Cone-beam computed tomography
(CBCT) imaging is best for showing the extent
of condylar damage from RA, particularly in
the early stages, and involves a lower radiation
dose than conventional CT scans.79 There is a
positive correlation between the duration and
severity of RA, and the degree of TMJ involve-
ment.78 Ankylosis of the TMJ is uncommon
and occurs late in the disease course.74 If
ankylosis or collapse of the TMJ occurs, joint
replacement may become necessary.74 This has
been shown to have good long-term outcomes
for patients with inflammatory arthritis.80
TMD management in RA needs to involve the
patient’s rheumatologist and an oral & maxillo-
facial surgeon with an interest in TMJ diseases.74
Juvenile idiopathic arthritis (JIA), also known
as juvenile rheumatoid arthritis, affects around
12,000 children in the UK.81 The reported
prevalence of TMJ arthritis in JIA ranges from
17 to 87%.82 Restricted mouth opening is the
most frequent clinical finding (28% of patients)
followed by masticatory muscle tenderness,
deviation of the mandible on opening, TMJ
tenderness and joint sounds.82 TMJ arthritis in
children can cause a disturbance of mandibular
growth and evident alterations in craniofacial
morphology and occlusion; features typically
seen include an increased profile convexity, a
steeper mandibular plane angle, mandibular
micrognathia and retrognathia.83
Inflammation occurs during the active phase
of JIA, which ultimately causes resorption of
the condyles.82 Damage to the condyles may
be present early on in JIA and progress, even
when clinical symptoms and signs are absent.82
The current gold standard method of imaging
in JIA to detect early arthritic changes in the
TMJ is magnetic resonance imaging (MRI)
with contrast.84 Patients with JIA should have
regular imaging of the TMJ and evaluation by
an orthodontist, even in the absence of TMD
signs and symptoms.82
Lastly, it is important to note that some
patients with RA/JIA will have TMD that is
unrelated to their inflammatory arthritis.
Table 2 Oral signs and symptoms of Sjögren’s Syndrome75,88,90,91
Signs Symptoms
Enlarged parotid glands Soreness
Absence of saliva pooling in floor of mouth Burning
Dry/cracked oral mucosa and lips Loss of/altered taste sensation
Mouth sores Difficulty with eating
Increased caries incidence (especially cervical) Difficulty with swallowing
Increased dental erosion Difficulty with speaking
Erythematous cobblestoned/fissured tongue Pain from denture-induced irritation
Atrophy of filiform papillae
Coated tongue (‘black hairy tongue’)
Candidosis
Halitosis
Difficulty with denture retention
Table 3 Suggestions to make dental visits more comfortable for RA patients93,94
Organise appointments at times more suitable for the patient’s condition; for
example, if they experience morning stiffness, schedule visits for the afternoon.
Before treatment Make shorter, more frequent appointments rather than lengthy visits where patients
can experience stiffness in the dental chair.
Book a treatment room with step-free access.
Adjust the dental chair and headrest to a comfortable position, as RA patients can get
considerable neck pain and stiffness during treatment.
Offer the patient a small pillow or allow them to bring their own.
During treatment Allow the patient to rest and move their jaw periodically during treatment to prevent
pain, fatigue and stiffness from keeping their jaw open for prolonged periods.
Reassure the patient that they can ask to take a break at any time.
Ask the patient if they require any other adjustments.
Salivary gland dysfunction within it (called mucins) which affect its ability
Sjögren’s syndrome (SS) is a chronic autoim- to retain water.87 Up to 70% of salivary mucins
mune condition that is characterised by the are produced by the minor salivary glands and
sicca symptoms xerophthalmia and xerostomia, overall they produce 10% of saliva.89 Therefore,
caused by inflammation leading to dysfunction currently available treatments aimed solely at
of the lacrimal and salivary glands.85 It can occur increasing salivary flow may not be sufficient
alone (primary form) or secondary to other to provide relief for SS patients.
systemic autoimmune diseases such as RA.86 Xerostomia can affect the oral cavity in many
The estimated prevalence of sicca symptoms in ways (see Table 2). Besides SS, a dry mouth
RA patients ranges between 30–50%.86 can also be caused by medications taken by RA
RA patients with SS have reduced salivary patients (see Table 1). It is important to note
flow and altered saliva composition (due to that xerostomia may be reported by patients
destruction and dysfunction of the salivary before obvious signs of hyposalivation are
glands).87 This reduces the buffering and antimi- visible in the mouth.87 If a patient presents
crobial properties of saliva causing an increased with a dry mouth and also complains of dry
likelihood of caries.88 The subjective experience eyes, it is worth writing to their general medical
of xerostomia in SS is not dependent on the total practitioner (GP), or rheumatologist if they
quantity of saliva (salivary flow) but rather the have a known rheumatic disorder, for further
quantity and quality of specific components investigation.

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Dental management Table 4 Summary of suggested management for RA-associated dental

General considerations
Most RA patients can be successfully managed
at the dental practice with some minor adjust-
ments – see Table 3 for suggestions. Chronic
inflammation of the cervical spine in RA can
result in neck instability, which can cause neu-
rological symptoms and in rare cases be fatal.92
It is therefore important that a patient’s head and
neck are well supported during dental treatment.
Suspected cervical instability should also be
discussed with the patient’s rheumatologist.
Due to pain, impaired hand function and
fatigue; RA patients may find it difficult and
lack the motivation to follow a good oral
hygiene regime (leading to further unfavour-
able outcomes).54,55,95,96 Good oral hygiene is the
cornerstone for dental management of these
patients, and aids should be recommended
to making brushing and interdental cleaning
easier for this population with poor grip and
dexterity. Resources on suitable aids and adapta-
tions are available.93,95 See Table 4 for a summary
of management of common RA-associated
dental problems. If a patient is having recurrent
problems due to their RA or medication, please
discuss this with their rheumatologist or GP.
problems74,75,77,88,90,91,93–95,97–100
Dental problem Management
More frequent dental/hygiene visits
Regular scaling and root planing (no adjuncts necessary)
Oral hygiene instruction – recommend electric toothbrushes and interdental cleaning
Periodontal disease
aids with wider handles
Smoking cessation advice and support
Refer to a periodontist if necessary
Jaw rest
Warm compress application
Physiotherapy
Soft food diet
Temporomandibular Short-term NSAID use (topical or systemic)
dysfunction Occlusal splint (soft or hard) wear at night time
Biobehavioural therapy
Elimination of unhelpful habits for example, nail biting, wide yawning
Discuss with patient’s rheumatologist/GP if TMJ arthritis suspected
Refer to oral & maxillofacial surgery and orthodontics (for children) if necessary
More frequent dental visits
Medication review
Advise to keep hydrated with regular sipping of water

Smoking cessation advice

Concurrent medications
As for any patient, it is important to take and
keep updated a thorough medical/surgical
history with a full medication list. Be aware of
drug interactions when prescribing (particu-
larly antibiotics); if in doubt consult the British
National Formulary.101 If prescribing NSAIDs,
check what the patient is already taking and
assess toxicity risk.94 Some RA patients take
oral bisphosphonates for the prevention or
treatment of osteoporosis; therefore, there is a
small risk (estimated at 0.5%) of osteonecrosis
of the jaw following dentoalveolar surgery.102
This risk can be increased with concomitant
use of corticosteroids, and in some cases
bisphosphonates may need to be stopped at
least two months prior to surgery.102 Biologic
DMARDs should be stopped much before
major surgical procedures (according to the
half-life of drug) so as not to increase infection
risk.6 Conventional DMARDs may need to be
stopped prior to procedures which last over
Chew sugar-free gum or lozenges regularly (if no TMJ problems)
Oral hygiene instruction
Pit and fissure seal teeth
Fluoride varnish, prescription-strength toothpaste or mouthwash
Salivary gland Use of non-fluoride remineralising agents for example, calcium phosphate rinse
dysfunction
Chlorhexidine varnish, gel or mouth rinse
Advise to reduce sugar/acid intake and frequency
Salivary replacement (gels, mouth rinses, toothpastes, lozenges)
Advise patient to use a humidifier, particularly when sleeping
Discuss with patient’s rheumatologist/GP
Prescribe salivary stimulants for example, pilocarpine
Refer to oral medicine if necessary
Refer to GP/rheumatologist if an undiagnosed underlying rheumatic disease is
suspected
Prescribe topical or systemic antifungals
Oral candidosis/
Discourage denture wear at night
angular cheilitis
Encourage good denture hygiene

an hour and it is recommended corticosteroid Check patient is taking medication (especially methotrexate) at the prescribed dose
and interval
exposure be minimised prior to surgery.103
Oral ulceration Prescribe benzydamine mouthwash/oromucosal spray
Therefore it is important to consult with the
patient’s rheumatologist well in advance of any Urgent referral to oral medicine if ulcers are longstanding (>3 weeks) or suspicious
planned invasive procedures and to follow up the
NSAID = Non-steroidal anti-inflammatory drug; GP = General medical practitioner; TMJ = Temporomandibular joint.
patient postoperatively.

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 GENERAL
Antibiotic and steroid cover
The National Institute for Health and Care
Excellence’s recently updated guidance is that
patients considered at high risk of infective
endocarditis do not routinely require antibiotic
prophylaxis for dental procedures, though this
may be appropriate in individual cases.104 If in
doubt, consult with the patient’s cardiologist.
Latest guidelines from the British Society of
Rheumatology state that pre-operative increase
in steroid dose, for adrenal crisis prevention, is
no longer routinely required.103 However, if a
patient shows signs of adrenal crisis (vomiting,
abdominal pain, syncope, low blood pressure,
hypoglycaemia, confusion) during a procedure,
seek immediate emergency medical attention.94
Co-morbidity detection
Dentists should be aware of the potential co-
morbidities with RA and refer patients on to an
appropriate medical professional for further inves-
tigation (copying in the patient’s rheumatologist
and GP) if they detect anything of concern.
Conclusion
RA is a multi-faceted disease which can be
complex to manage as co-morbid conditions
are frequently present. Dental complications
can arise associated with RA or its treatment.
It is important that the dental team are aware
of them so these patients can be successfully
managed in general dental practice, with early
intervention to prevent a further decline in
their quality of life. Simple adjustments can be
made to make dental visits more comfortable
for patients with this long-term condition.
Acknowledgements
The authors would like to thank Tina Alvand,
Rajvi Haria, Hiten Joshi, Heidi Lempp, Lydia Pink,
Miranda Steeples and Ruth Williams for their
manuscript feedback.
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